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"Istvanffy, Peter"
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Exceptional life journeys : stories of childhood disorder
\"Most students in training to become teachers, psychologists, physicians, and social workers as well as many practicing professionals in these disciplines do not get the opportunity to fully understand and appreciate the circumstances of children, parents, and teachers who have had to cope and adapt to childhood disorder. Most professionals in the field of childhood disorders are well trained in assessment and treatment methods and are aware of the clinical, theoretical, and empirical foundations of the work they do. In their training, they get some experience in diagnosing the educational, psychological, social, and medical problems of children through their supervised clinical internships. In their training and in their professional practice they get to interview, discuss, consult and collaborate with children and their families regarding developmental issues and treatment plans, however, they rarely get an opportunity to fully realize and understand what it is like to have a disorder and what it is like to be a mother, or father, or teacher of children with disorders. This book provides an opportunity for students in training and professionals in the field to gain some awareness of the life journeys of some exceptional children, their families and their teachers.\"--Publisher's website.
Book
Genetic alterations of the SUMO isopeptidase SENP6 drive lymphomagenesis and genetic instability in diffuse large B-cell lymphoma
SUMOylation is a post-translational modification of proteins that regulates these proteins’ localization, turnover or function. Aberrant SUMOylation is frequently found in cancers but its origin remains elusive. Using a genome-wide transposon mutagenesis screen in a MYC-driven B-cell lymphoma model, we here identify the SUMO isopeptidase (or deconjugase) SENP6 as a tumor suppressor that links unrestricted SUMOylation to tumor development and progression. Notably,
SENP6
is recurrently deleted in human lymphomas and SENP6 deficiency results in unrestricted SUMOylation. Mechanistically, SENP6 loss triggers release of DNA repair- and genome maintenance-associated protein complexes from chromatin thereby impairing DNA repair in response to DNA damages and ultimately promoting genomic instability. In line with this hypothesis, SENP6 deficiency drives synthetic lethality to Poly-ADP-Ribose-Polymerase (PARP) inhibition. Together, our results link
SENP6
loss to defective genome maintenance and reveal the potential therapeutic application of PARP inhibitors in B-cell lymphoma.
SUMOylation is a post-translational modification that has been shown to be altered in cancer. Here, the authors show that loss of the SUMO isopeptidase SENP6 leads to unrestricted SUMOylation and genomic instability promoting lymphomagenesis and generating vulnerability to PARP inhibition.
Journal Article